Background To determine the binding activity of nuclear factor-KB (NF-KB) and the transcription of transforming growth factor-pi (TGF-β1) induced by oxidized low density lipoprotein (Ox-LDL) in rat mesangial cells and to elucidate the mechanism of renal injury of Ox-LDL.Methods NF-KB binding activity was measured by gel shift assay in mesangial cells with or without inducement of Ox-LDL. Protein kinase inhibitors and activtors were then used to determine the signal transduction pathways. In this course IKB protein expression was analyzed by Westerm blot assay. TGF-β1 mRNA was measured in mesangial cells exposed to Ox-LDL by RT-PCR assay. TGF-β1 promoter from -1551 to +57 were constructed into a pGL3-Basic vector with a luciferase reporting gene. A putative binding site of NF-KB was mutated. The wild and mutant promoters activity was analyzed by transfection into mesangial cells.Results NF-KB was activated by Ox-LDL persistently and rebounded in the early period. Ox-LDL induced NF-KB activation in a d Background To determine the binding activity of nuclear factor-KB (NF-KB) and the transcription of transforming growth factor-pi (TGF-β1) induced by oxidized low density lipoprotein (Ox-LDL) in rat mesangial cells and to elucidate the mechanism of renal injury of Ox-LDL. Methods NF-KB binding activity was measured by gel shift assay in mesangial cells with or without inducement of Ox-LDL. Protein kinase inhibitors and activtors were then used to determine the signal transduction pathways. IKB protein expression was analyzed by Westerm blot assay. TGF-β1 mRNA was measured in mesangial cells exposed to Ox-LDL by RT-PCR assay. TGF-β1 promoter from -1551 to +57 were constructed into a pGL3-Basic vector with a The luciferase reporting gene. A putative binding site of NF-KB was mutated. The wild and mutant promoters activity was analyzed by transfection into mesangial cells. Results NF-KB was activated by Ox-LDL persistently and rebounded in the early period. Ox-LDL induced NF-KB activation in a d